Background: Inflammatory bowel disease (IBD) is originated from uncontrolled inflammation, and desired methods for IBD therapy remains the main difficult. The network comprised with miRNA and 1ncRNA has been verified to play an important role on diverse human diseases. In this study, we demonstrated the role of miR-34c and lncRNA PIncRNA1 on the function of intestinal barrier. Methods: Intestinal epithelial barrier model was constructed based on normal intestinal epithelial cell line Caco-2. 2% DSS was supplemented in the Apical side of the model cells to induce the injury of intestinal epithelial barrier. Real-time PCR or western blot was used to determine mRNA or protein expression of miR-34c, PIncRNA1, Myc-associated zinc finger protein (MAZ), zonula occludens 1 (ZO-1) and occludin. Results: DSS induced injury of intestinal epithelial barrier, while overexpression of PIncRNA1 seemed to protect intestinal epithelial barrier from injury. Tight junction (TJ) proteins ZO-1 and occludin were regulated by MAZ, while, miR-34c targeted MAZ to regulate its expression, in addition, PIncRNA1 and miR-34c bound together to regulate the expressions of MAZ, ZO-1 and occludin. The protect effects of PIncRNA1 overexpression on intestinal epithelial barrier function was reversed by overexpression of miR-34c. Conclusion: MAZ and TJ proteins were involved in the function of intestinal epithelial barrier, while miR34c and PIncRNA1 regulated the intestinal dysfunction cooperatively. (C) 2017 Published by Elsevier Inc.